Fluid shear regulation of local Ca ²⁺ transients in right and left rat atrial myocytes under normal and increased beating rate

During volume increase or hemodynamic disturbances in the atrium, fluid shear and beating rate often increase. Shear stress induces Ca 2+ waves in resting atrial myocytes. Here, we examined whether shear stress alters local Ca 2+ signaling and how such shear adaptation changes with increased beating frequency in right atrial (RA) and left atrial (LA) myocytes. Using two-dimensional confocal Ca 2+ imaging in combination with micro-puffing, we examined the spatiotemporal properties of junctional (peripheral) and non-junctional (central) Ca 2+ signals in field-stimulated rat atrial myocytes. Shear stress (~16 dyn/cm 2 ) immediately enhanced Ca 2+ transients, with a larger effect in the center, followed by their inhibition. During the early stimulatory phase only, Ca 2+ release and decay were prolonged, with greater lengthening in the periphery. Whereas no difference was observed between RA and LA shear responses at 1 Hz, larger stimulatory effects were observed in RA myocytes than in LA myocytes at 3 Hz, with no late inhibition. At 3 Hz, only RA myocytes showed early shear-induced prolongation of Ca 2+ release in the periphery. Sarcoplasmic reticulum (SR) Ca 2+ contents were similarly reduced by prolonged shear in both sides at 1- and 3-Hz. Increased frequency caused attenuations in Ca 2+ transients and peripheral SR Ca 2+ content in LA, but not RA, myocytes under control conditions. Our data suggest that shear stress transiently enhances central Ca 2+ release during depolarization via prolonged peripheral release but later suppresses it, and that early shear-mediated Ca 2+ release stimulation deteriorates more readily in LA myocytes at increased frequencies, partly due to a reduced peripheral store.